PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Polyomavirus”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2026

Binding capacity of Intravenous immunoglobulin G to BK polyomavirus determines its anti-BK polyomavirus activity in infected cultures.

BK polyomavirus (BKPyV) causes disease in immunocompromised individuals. This study tested the hypothesis that the antiviral efficacy of intravenous immunoglobulin (IVIG) against BKPyV depends on the relationship between its virus-binding capacity and the viral burden. We first quantified the BKPyV-binding capacity of IVIG and then characterized BKPyV replication in kidney-derived HK-2 and HEK293&#x202f;cells and in HEL cells under IVIG treatment. Subsequently, we analyzed the efficacy of IVIG at 0.03-10&#x202f;mg/mL against low-multiplicity of infection (MOI) and high-MOI infection in relation to the BKPyV-binding capacity of IVIG. BKPyV productively infected all three cell lines, with 14-day replication cycles of 2.2, 4.0, and 7.0 in HK-2, HEK293, and HEL cells, respectively, indicating that HEL cells were the most permissive. IVIG bound approximately 108 copies of BKPyV DNA per milligram. In the low-MOI infection model, where the total viral load remained within this estimated binding capacity, IVIG showed clear neutralizing activity, significantly reducing viral spread, viral DNA levels, and the number of VP1-positive cells in a dose-dependent manner (p&#x202f;<&#x202f;0.001). In contrast, in the high-MOI infection model, the viral load appeared to be high relative to the estimated IVIG binding capacity even at 10&#x202f;mg/mL, and IVIG showed little or no neutralizing effect on viral production or spread of infected cells. These findings identify an experimental relationship between IVIG binding capacity, viral burden, and antiviral efficacy and suggest that the antiviral effect of IVIG is greatest when administered early, thereby supporting further clinical evaluation of early or preemptive IVIG administration.

Humans↗
PubMed1975

Evidence of chronic persistent infections with polyomaviruses (BK type) in renal transplant recipients.

Ten renal transplant recipients showing a significant increase in human polyomavirus antibodies, indicative of an acute infection, were followed up serologically over periods ranging from two months to more than two years. Fifty-four serum specimens were available for the study and they were tested by both haemagglutination-inhibition and complement-fixation. Polyomavirus antigens were prepared from the BK and SV40-like strains of polyomaviruses, and from the SV40 virus. One strain of polyomavirus, related to the BK strain was isolated from the urine of one of these patients. Two other BK strains were recovered from the urine and kidney, respectively, of transplant recipients not included in this study. Sera of these two patients were not obtained until the transplantation was made; they were already highly positive for polyomavirus antibodies, precluding the demonstration of an increase in antibody titer. Serologic results have shown that HAI antibodies persist at high titers throughout the observation period. This persistence ranged from two to four months (four cases), seven to eleven months (three cases) and thirteen to twenty months (three cases). In none of the cases could a decrease of high titer be demonstrated. Moreover, density gradient studies have shown that specific IgM antibodies also tend to persist over many months. Similar serologic results were obtained in complement-fixation tests with a BK antigen. Titers were at least 1 in 30 in the study group, but were not observed among healthy blood donors. All sera were uniformly negative for SV40 and SV40-like antigens. One polyomavirus isolation was successful from urine obtained six months after initial serologic evidence for a polyomavirus infection. The other two viruses were isolated from materials taken four and seven months after first detection of polyomavirus antibodies at high titer. Both serologic evidence and viral isolations seem to indicate that polyomaviruses (BK type) might cause a chronic infection in humans.

Animals↗
PubMed2025

Temporal gating of nuclear import: How Merkel cell polyomavirus exploits the cell cycle for nuclear entry.

Merkel cell polyomavirus (MCPyV) is a small, DNA tumor virus that is causally linked to an aggressive form of human skin cancer called Merkel cell carcinoma. MCPyV is the only polyomavirus definitively shown to cause cancer in humans, yet little is known about how it establishes infection in target cells. In this study, we report an unconventional mechanism by which MCPyV enters the host cell nucleus, where viral genome replication occurs. We demonstrate that, unlike other known polyomaviruses, MCPyV does not require the nuclear pore complex during entry. Instead, it takes advantage of cell cycle-dependent nuclear envelope breakdown to deliver its genetic material into the nucleus. We further show that the VP1 major capsid protein is sufficient to facilitate this process. Overall, our findings reveal a novel mechanism of polyomavirus nuclear entry and provide insight into the diverse mechanisms that these viruses use to cause infection.

Merkel cell polyomavirus↗
PubMed1979

Influence of inactivated Sendai virus on early events in polyomavirus infection of permissive and nonpermissive host cells.

Quantitative radiochemical investigations have been performed regarding the influence of betapropiolactone-inactivated Sendai virus on the early events of interaction of polyomavirus with permissive and nonpermissive cells. These experiments have shown: (i) Sendai virus did not increase polyomavirus adsorption on permissive or nonpermissive cells; (ii) Sendai virus induced polyomavirus elution from permissive and nonpermissive cells during the first 40 min and 6 h postinfection, respectively; and (iii) Sendai virus promoted the penetration of polyomavirus into lysosomes only in nonpermissive cells. The maximal amounts of radioactively labeled virion DNA and viral coat proteins were found in lysosomes at 2--3 h postinfection.

Adsorption↗
PubMed2025

Identification of Novel Wraparound Transcripts in JC Polyomavirus.

JC polyomavirus (JCPyV) is a ubiquitous pathogen that causes progressive multifocal leukoencephalopathy (PML). Although a recent study using next-generation sequencing (NGS) provided detailed transcriptome atlases for polyomaviruses (PyVs) such as BK polyomavirus and simian virus 40, the transcriptome of JCPyV remains poorly characterized. Here, we conducted a comprehensive analysis using both short-read and long-read NGS technologies to construct a transcriptome atlas of JCPyV. RNA extracted from IMR-32 and HEK293 cells transfected with the circular JCPyV genome was analyzed, leading to the identification of 39 previously uncharacterized viral transcripts in addition to 12 known ones. Among the novel transcripts, we identified wraparound transcripts, conserved across PyVs, which are generated through continuous, multicyclic transcription of the circular viral genome. These included both late transcripts containing leader-to-leader repeated sequences and SuperT transcripts with multiple LxCxE motifs. Notably, wraparound transcripts, including SuperT transcripts, were also detected in brain tissues from PML patients. Collectively, this study significantly expands our understanding of the JCPyV transcriptome, revealing the expression of wraparound transcripts in PML lesions. These findings provide valuable insights into the molecular basis of JCPyV gene expression and PML pathogenesis, potentially facilitating the development of effective countermeasures against PML.

JC Virus↗
PubMed1978

Brain tumors in owl monkeys inoculated with a human polyomavirus (JC virus).

Owl monkeys were inoculated intracerebrally, subcutaneously, and intravenously with JC, BK, or SV40 virus. Two of four adult owl monkeys inoculated with JC virus, a human polyomavirus, developed brain tumors at 16 and 25 months after inoculation, respectively. A grade 3 to grade 4 astrocytoma (resembling a human glioblastoma multiforme) was found in the left cerebral hemisphere and brainstem of one monkey. The second monkey developed a malignant tumor in the left cerebral hemisphere containing both glial and neuronal cell types. Impression smears prepared from unfixed tissue of this tumor showed cells that contained polyomavirus T antigen. Virion antigens were not detected. Tumor cells cultured in vitro also contained T antigen but were negative for virion antigen. Infectious virus was not isolated from extracts of this tumor.

Antibodies, Viral↗
PubMed2026

Single-cell profiling reveals epithelial and immune responses in BK polyomavirus-infected human kidney biopsies.

INTRODUCTIONBK polyomavirus (BKV) infection is associated with injury and subsequent graft loss due to the extent of injury or rejection. However, the molecular mechanisms driving injury and subsequent adverse outcomes remain poorly understood.METHODSIn a cross-sectional study, single-cell RNA-seq from kidney allograft biopsies was used to assess cell type-specific responses between uninfected controls and 2 distinct phases of BKV infection: peaking (increasing viral blood titers) and resolving (decreasing viral titers following immunosuppression reduction).RESULTSGenes upregulated in BK viral nephropathy (BKVN) were enriched for polyomavirus infection hallmarks, including ribosome biogenesis, translation, and energy restructuring. Additionally, enriched pathways included wound healing, cellular stress, antigen presentation and immune signaling. Even without BKVN (peaking BK viremia alone), epithelial cells expressed signatures for wound healing, cellular stress, and extracellular matrix remodeling. In vivo tubular cell responses at single-cell resolution were validated against single cell transcriptomic data of BKV-infected cells in a cell culture model. Despite similarities, in vivo tubular cells underwent metabolic adaptation favoring fatty acid oxidation and proinflammatory responses not observed in culture models, likely due to an absent innate and adaptive immune system. Despite lymphopenia and immunosuppressive therapies, the proportion of recipient-derived intrarenal adaptive immune cells was increased in biopsies associated with peaking viremia alongside activation of innate immune responses. Adaptive immune cells exhibited persistent inflammatory signaling and remodeling of energy metabolism during the resolving phase of infection.CONCLUSIONThese not previously reported insights into BKV-associated injury may have implications for clinical management and improved allograft outcomes.

Humans↗
PubMed1979

Isolation of polyomavirus-induced surface antigens of mouse cells: affinity chromatography and biologic activities.

Tumor-specific transplantation antigen (TSTA) and polyomavirus-induced tumor-associated surface antigen (TASA) were isolated from polyomavirus-transformed BALB/c mouse cells with the use of 3-M KCl solubilization and affinity chromatography on antibody-coated Sepharose 4B. Particular conditions were chosen for removal of the nonspecifically bound proteins from the gel. Under these conditions, the ratio between the amounts of crude extract and specifically bound proteins giving the same TASA activity was about 5,000. Mice inoculated with this material were protected against tumor challenge. We therefore assume that TSTA is a part of TASA. Furthermore, these antigens can be dissociated from the major histocompatibility antigens.

Animals↗
PubMed1978

Human polyomavirus (BK) infection and ureteric stenosis in renal allograft recipients.

Human polyomavirus (BK) was detected in two renal allograft recipients as a result of routine examination of Papanicolaou-stained smears of urinary sediment in the light microscope. Infection with this recently identified virus was confirmed by virus isolation and electron microscopy. The cytological, histological, and ultrastructural changes due to the virus are described, and virus excretion is correlated with the clinical progress of the patients and the pathological findings. The transplant ureters in both patients were found to be ulcerated and stenosed, and virus-infected cells were observed in the ureteric epithelium. We suggest that the administration of high-dose steroids in transplantation may permit active infection with human polyomavirus to occur in ureteric epithelium which has been damaged by ischaemia or inflammation.

Animals↗
PubMed2026

Genetic Diversity of BK Polyomavirus Among Renal Transplant Recipients in Yunnan, China.

BK polyomavirus (BKV) infection, a common complication following kidney transplantation, can lead to BKV-associated nephropathy (BKVN). Molecular genetic studies have classified BKV into four genotypes (I-IV); however, comprehensive molecular characterization of BKV strains circulating in China remains limited. This study aimed to elucidate the predominant subtypes and clinical infection characteristics of BKV strains among kidney transplant recipients in Yunnan, a province in southwestern China. PCR-amplified BKV DNA sequences from kidney transplant recipients were aligned with reference strains and subjected to phylogenetic analysis. The viral VP1 gene was successfully amplified from 180 participants, spanning 16 ethnic groups. Genotype I was the predominant viral strain (56.66%, 102/180), followed by genotype IV (43.33%, 78/180), while genotypes II and III were not detected. Among genotypic subtypes, IVc-1 was most prevalent (40.0%, 72/180), followed by Ic (38.3%, 69/180) and Ib-1 (18.3%, 33/180). IVa-1 and IVa-2 were rare, identified in only 0.6% (n&#x2009;=&#x2009;1) and 2.2% (n&#x2009;=&#x2009;4) of cases, respectively. No significant differences in sex, age, BKVN incidence, BK viremia, or viruria were observed between patients with BKV-I and BKV-IV infections. Among the five confirmed BKVN cases, two were genotyped as subtype Ic, one as Ib-1, and two as IVc-1. Clinical phenotypes were also comparable between patients with BKV-I and BKV-IV infections. This study represents the largest single-center sequencing analysis of BKV in kidney transplant recipients in China, offering a valuable genomic resource for future research.

Humans↗
PubMed1988

Cooperation between the polyomavirus middle-T-antigen gene and the human c-myc oncogene in a rat thyroid epithelial differentiated cell line: model of in vitro progression.

Two rat thyroid epithelial differentiated cell lines, PC Cl 3 and PC myc, were infected with the polyoma murine leukemia virus (PyMLV) carrying the Middle-T-antigen gene of polyomavirus. After infection, both cell lines acquired the typical markers of neoplastic transformation; however, the PC myc cells showed a greater malignant phenotype. Furthermore, the thyroid differentiated functions were completely suppressed in PC myc cells transformed by PyMLV, whereas they were, at least partially, retained in PC Cl 3 cells transformed by PyMLV, and in particular, thyroglobulin synthesis and secretion were not affected at all. Since no differences in the expression of the middle-T-antigen gene were observed in the two PyMLV-transformed cell lines, the different properties shown by these two infected cell lines must be ascribed to the expression of the c-myc oncogene.

Animals↗
PubMed1977

JC virus, a human polyomavirus associated with progressive multifocal leukoencephalopathy: additional biological characteristics and antigenic relationships.

JC virus, a human polyomavirus, failed to grow or produce cytopathic effects in any of a variety of cells tested other than primary human fetal glial (PHFG) cells. Cells tested included other primary human cells and glial cells from other animals. Only a rare cell in inoculated insusceptible human cell cultures produced T or virion antigen. In PHFG cell cultures JC virus produced subtle cytopathic effects, and the majority of progeny remained cell associated. Only a few cells in the heterogenous PHFG cell cultures contained T antigen at 24 h postinoculation, and virion antigen was not detected until 48 h postinoculation. The infectivity of JC virus was resistant to inactivation by ether and by heating at 50 degrees C for 1 h. A three-way minor antigenic relationship was demonstrated among the virion antigens of JC virus, BK virus, and simian virus 40 by neurtralization and/or hemagglutination inhibition tests. Serological evidence is presented for the existence of JC virus as a distinct entity before the use of simian virus 40-contaminated poliovirus vaccines and for the nonexistence of an animal reservoir for JC virus infection.

Animals↗
PubMed2026

Benchmarking urinary cell transcriptomes for noninvasive differentiation of BK polyomavirus-associated nephropathy from T cell-mediated rejection.

BK polyomavirus-associated nephropathy (BKVN) adversely impacts kidney allograft survival and often mimics acute T cell-mediated rejection (TCMR), confounding diagnosis and management. To address this conundrum, we performed unbiased RNA sequencing of urinary cells matched to biopsies classified as BKVN with intragraft inflammation (BKVN-P), BKVN without inflammation (BKVN-N), TCMR, or no rejection (NR). BKVN-N displayed dominant host DNA replication, cell cycle, and repair programs, while BKVN-P samples exhibited expansive innate immune activation, antigen presentation, chemokine upregulation, and epithelial injury. Both BKVN subtypes shared signatures of T cell exhaustion and mature and tolerogenic dendritic cell activation but differed in immune orientation - Th1 predominance in BKVN-N versus Treg and CD8 enrichment in BKVN-P. Compared with TCMR samples, BKVN-P lacked robust TCR/CD28 signaling and was enriched for viral and innate modules; BKVN-N lacked alloimmune activation. B cell exhaustion characterized BKVN-N, while BKVN-P displayed robust B cell activation with metabolic downregulation. A ratiometric urinary cell biomarker, CXCL10 mRNA/CD3E mRNA, distinguished both BKVN subtypes from TCMR with diagnostic accuracy, replicated by quantitative reverse transcription PCR for clinical translation, and confirmed in an independent cohort. These findings demonstrate the utility of urinary cell transcriptomics for resolving viral injury from alloimmunity, enabling precision diagnostics and targeted immunomodulation in kidney transplantation.

Humans↗
PubMedDate not supplied

[Effect of inactivated Sendai virus on polyomavirus adsorption and penetration].

The quantitative study of adsorption, elution, and penetration of oncogenic polyoma virus (PV) labeled with 3H-thymidine under the influence of beta-propiolactone-inactivated Sendai virus (SV) was carried out in a permissive culture of mouse embryo fibroblasts and in two nonpermissive cultures of human embryo and chick embryo fibroblasts. In adsorption of PV on permissive and nonpermissive cells SV was found to reduce the amount of the adsorbed virus if used before the adsorption and to have no effect on adsorption upon reverse order of treatment of the cells with the two viruses. SV facilitates elution with 5 mM EDTA of PV adsorbed on both permissive and nonpermissive cells. Under the influence of SV, PV could be eluted from the surface of the permissive cells within 1 hour after adsorption and from the surface of the nonpermissive cells within 5-6 hours. Three hours after PV adsorption on permissive cells, both treated and untreated with SV, most of PV DNA (approximately 60%) was found in the nuclear fraction. At the same time, in the nuclear fraction of nonpermissive cells, treated or untreated with SV, the amount of PV DNA was insignificant (about 13%). The fraction containing large granules isolated from the cells which had been in contact with SV was found to contain approximately 50% of 3H-thymidine label.

Adsorption↗
PubMed1978

[Transformation of human embryonic cells by the Rous sarcoma virus and the polyomavirus depending on the mitotic cycle phase].

The whole cycle of skin-muscle embryonic human tissue culture is 18 hours, with phases S, G1, G2 and M being 7, 6, 4 and 1 hour, respectively. The mitotic index of this culture is 28%. The maximum sensitivity of these synchronized cell cultures to transforming activity of the Rous and Sindai viruses was observed in phase S. The infection of synchronized primary embryonic human fibroblasts in phase S with the polyoma virus together with the Sindai virus has resulted in single cases of transformation. Similar results were obtained with non-synchronized human cultures.

Adsorption↗
PubMed1979

A rapid method for detecting and mapping homology between heterologous DNAs. Evaluation of polyomavirus genomes.

A new approach for evaluating homologous sequences among related DNAs is presented. Conventional filter hybridization techniques are employed at 35 degrees C in a range of formamide concentrations in order to perform annealings at effective temperatures as low as Tm -50 degrees C which permits the detection of regions of homology with as much as 33% base mismatch. Under such nonstringent conditions, high levels of specific annealing can be obtained at plateau levels. In combination with the Southern "blotting" technique (1975), this approach can be used to perform biochemical heteroduplex melting experiments. The homology among the genomes of the murine polyoma virus (Py), the simian virus 40 (SV40), and the human papovavirus BK was evaluated using this new methodology.

DNA, Viral↗